粘连性肩关节囊炎的治疗(二)
英语晨读 ·
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本次文献选自Redler LH, Dennis ER. Treatment of Adhesive Capsulitis of the Shoulder. J Am Acad Orthop Surg. 2019;27(12):e544-e554. 本次学习由阎芳副研究员主讲。
Pathology
The exact pathophysiology of AC is not completely understood and is often idiopathic. The main pathology is thought to involve inflammatory contracture of the shoulder capsule with recruitment of inflammatory cytokines such as transforming growth factor beta (TGF-b), tumor necrosis factor alpha (TNF-a), and interleukins, as well as B-lymphocytes, T-lymphocytes, and macrophages. One study examining the histology of excised CHL found active fibroblastic proliferation with some transformation to myofibroblasts, creating collagen in the form of a thick band, similar in appearance to Dupuytren’s disease. This transformation to smooth muscle myofibroblasts is thought to cause contracture, capsular hyperplasia, and eventual fibrosis which is thought to cause reduction in capsular volume and stiffness, ultimately restricting motion. In summary, AC appears to start as an inflammatory reaction with associated synovitis that progresses to fibrotic contracture of the shoulder capsule.
病理
AC的确切病理生理学还不完全清楚,通常是特发性的。其主要病理学表现为肩关节囊炎性挛缩,炎症细胞因子如转化生长因子β、肿瘤坏死因子α和白介素以及b淋巴细胞、T淋巴细胞和巨噬细胞聚集。一项研究对切除的喙肱韧带进行组织学检查发现,成纤维细胞增生活跃,一些成纤维细胞转化为肌成纤维细胞,形成厚带样的胶原,与杜普顿病的表现相似。这种向平滑肌肌成纤维细胞的转化可能会导致挛缩,关节囊增生,最终纤维化,这会引起关节囊体积减少,硬度增加,最终限制运动。综上所述,AC似乎是一种炎症反应,逐渐由滑膜炎发展为肩关节囊的纤维化挛缩。
Classification
As previously described by Neviaser and Neviaser, AC is classified into four stages based on arthroscopic and histologic appearance of the joint capsule, following progression from capsular inflammation to fibrosis (Figure 1). Stage 1, “the preadhesive stage,” is described as proliferation of the fibroblasts without formation of adhesions. Patients have full ROM but report pain, often at night. Stage 2, “acute adhesive synovitis,” is characterized by hypertrophy of the synovium and early formation of adhesions, often in the inferior capsular fold. Patients begin to have mild loss of ROM with pain. Stage 3, “the maturation stage,” is marked by the transition of synovitis to fibrosis. The axillary fold is often adhered to the capsule. ROM becomes markedly reduced, but often patients are in less pain than in the earlier stages. Stage 4, “the chronic stage,” is characterized by severe loss of ROM and dense fibrotic adhesions. Of note, stage 4 patients can have minimal pain, except when their ROM is forcefully moved past the restraints of their fibrotic capsule.
分类
正如Nevaser和Nevaser之前所描述的,AC根据关节囊的关节镜下和组织学表现分为四个阶段,从关节囊炎症发展到纤维化(图1)。第一阶段,“粘连前阶段”,是指成纤维细胞增殖而不形成粘连。患者肩关节活动度正常,但主诉疼痛,夜间尤甚。第2阶段,“急性粘连性滑膜炎”,以滑膜肥厚和早期粘连形成为特征,常发生在下囊襞。病人开始有轻度活动受限,伴疼痛。第3阶段,“成熟期”,以滑膜炎向纤维化转变为特征。腋窝皱襞通常附着在关节囊上。肩关节活动度明显减少,但患者疼痛通常比早期减轻。第4阶段,“慢性期”,以严重活动受限和致密的纤维粘连为特征。值得注意的是,第 4 阶段患者的疼痛可能很轻,除非他们的运动范围被强行移动超过纤维化囊的限制。
In describing AC to patients, the senior author finds it helpful to break the progression down into three clinical phases based on the overlapping nature of inflammation and scar tissue formation as described by Neviaser and Hannafin(Figure 1). Phase 1 involves only inflammation, characterized by capsular pain with sudden shoulder motion, usually in a functional range (not extremes), but patients do not yet have restricted ROM. Often, only patients who have suffered AC on the contralateral side present this early. Phase 2 involves both inflammation and scar tissue formation. Patients classically have pain and restricted ROM. This is the most common phase at presentation. Phase 3 is distinguished by the resolution of inflammation. Patients have profound loss of motion but often no longer have pain.
在向患者描述 AC 时,作者发现根据 Neviaser 和 Hannafin所描述的炎症和瘢痕组织形成的重叠性质,可以将肩周炎的进展分解为三个临床阶段(图 1)。 第 1 阶段仅涉及炎症,其特征是肩关节突然运动时出现关节囊疼痛,通常在功能范围内(不是终末端疼痛),但患者的活动度尚未受限。通常,只有对侧曾患肩周炎的患者才会出现这种早期症状。 第 2 阶段涉及炎症和疤痕组织形成。患者通常有疼痛和活动范围受限。这是最常见的疾病阶段。第 3 阶段的特点是炎症消退。患者有严重的运动障碍,但通常不再有疼痛。